tag:blogger.com,1999:blog-48260231491394262512018-12-19T06:32:11.292+00:00AntiCancerCommentary on cancer research, information on supplements and treatments, relevant book reviews, links to useful sites and other information that cancer sufferers, their families and friends may find useful.Pan Pantziarkanoreply@blogger.comBlogger154125tag:blogger.com,1999:blog-4826023149139426251.post-73876838653011408822018-06-19T08:31:00.001+01:002018-06-19T09:39:43.354+01:00Book Review - SCAM: So-called Alternative Medicine<div dir="ltr" style="text-align: left;" trbidi="on"><table border="0" style="width: 100%px;"><tbody><tr> <td><b>Keywords:</b> Homeopathy, alternative medicine<br /><b>Title:</b>SCAM: So-called Alternative Medicine<br /><b>Author:</b> Edzard Ernst<br /><b>Publisher:</b> Imprint Academic<br /><b>ISBN:</b> 978-1845409708 </td> <td></td> <td><div align="center"><img alt="cover" border="1" src="http://images-eu.amazon.com/images/P/1845409701.02.LZZZZZZZ.jpg" height="200" width="150" /><br /><br /><a href="http://www.amazon.com/exec/obidos/ASIN/1845409701/techbookrepor-20"><b>Buy US</b></a><br /><a href="http://www.amazon.co.uk/exec/obidos/ASIN/1845409701/454"><b>Buy UK</b></a></div></td> </tr></tbody></table><br />‘SCAM – So-called Alternative Medicine’, is the follow-up book to ‘<a href="http://www.anticancer.org.uk/2015/02/book-review-scientist-in-wonderland.html" target="_blank">A Scientist In Wonderland</a>’, Edzard Ernst’s very readable memoir. That book, reviewed <a href="http://www.anticancer.org.uk/2015/02/book-review-scientist-in-wonderland.html" target="_blank">here</a> previously, Ernst told the story of how he came to be the first Professor of Complementary Medicine in the world. It was a post that was greeted enthusiastically by those who were true believers in homeopathy, healing crystals and other forms of ‘alternative medicine’. These true believers assumed that anyone taking on that role would be like minded. Unfortunately, Ernst decided that he was a scientist first and foremost and that his job meant applying the scientific method to the extraordinary claims made by practitioners. The fall out reached a peak with a very public falling out with Prince Charles and trouble for Ernst from his own university. It’s an interesting story well-told in the first book.<br /><br />In this book Ernst is continuing the work that got him into so much trouble. Here he outlines how these various alternatives seem to work – their common features, imperviousness to evidence, the magical thinking and conspiracy theories that believers use to counter the lack of evidence. For example, many alternatives claim that much of contemporary medicine also doesn’t stack up and hasn’t been tested vigorously in clinical trial. While there’s a smidgen of truth there, Ernst points to the evidence that in conventional practice 80% - 90% is evidence-based (and includes the reference so you can look at the original paper itself).<br /><br />While the book lacks the narrative from the first – after all that was a memoir – it does run over some of the elements of his own experience in battling with Prince Charles. It’s a book that is informed by long experience talking to people who really do believe in homeopathy and so on. Some of the people who peddle this stuff really do believe it and have the best of intentions. But there are some very cynical, mercenary people who are driven entirely by selfish reasons to exploit vulnerable people when they are sick. But perhaps, as Ernst suggests here, there’s a third group – people who convince themselves and make a nice living at the same time.<br /><br />Overall this is certainly an interesting read – with plenty of useful information with which to counter fraudsters and fakes. There’s even a section on how to set yourself up as a charlatan – yep, you too can claim to cure cancer, fight dementia and tackle bad breath.</div>Pan Pantziarkanoreply@blogger.com0tag:blogger.com,1999:blog-4826023149139426251.post-23225182684621049212018-03-20T08:15:00.000+00:002018-03-20T08:15:00.966+00:00Wisdom of Crowds<div dir="ltr" style="text-align: left;" trbidi="on"><div class="separator" style="clear: both; text-align: center;"></div><br /><div class="MsoNormal">‘The Wisdom of Crowds’ is the name of a book by James Surowiecki in which he discusses the idea that in certain situations aggregating the knowledge from a random crowd of people could get to a better answer to a problem than any single individual could – even an expert individual. It wasn’t a new idea – according to Wikipedia (never a reliable source, so not a good ‘crowd’ example) that in 1907 Francis Galton noted that a crowd at a county fair correctly guessed the weight of an ox when you took the average of all the guesses. <span style="mso-spacerun: yes;">&nbsp;</span>Surowiecki’s book certainly popularised the term – I even used it in the title of a paper on drug repurposing: ‘<a href="https://ecancer.org/journal/editorial/50-the-wisdom-of-crowds-and-the-repurposing-of-artesunate-as-an-anticancer-drug.php" target="_blank">The wisdom of crowds and the repurposing of artesunate as ananticancer drug</a>’ – and it has become something of a standard feature of many books and courses in machine learning and data science.<o:p></o:p></div><div class="MsoNormal"><br /></div><div class="MsoNormal">The Nobel prize-winning economist and political scientist Frederich von Hayek didn’t, as far as I know, use the term but the idea was central to his thinking. He saw the price/market system as the wisdom of the crowds in action. He saw the society as a complex and self-organised system, with distributed decision making and dispersed knowledge as they key driving forces. Trying to control an economy from the top down is impossible without access to all that knowledge - knowledge that we are often not even explicitly aware that we have.<o:p></o:p></div><div class="MsoNormal"><br /></div><div class="MsoNormal">I’ve often wondered though whether it really works in practice, or was it really the case that yet again the world is far too complex and messy for even this simple (and surprising) idea to work. At the weekend I finally managed to see a real world example. In the context of some fundraising for the <a href="http://www.tp53.co.uk/" target="_blank">George Pantziarka TP53 Trust</a> (the UK charity that supports people with Li Fraumeni Syndrome), we attended the modern equivalent of Galton’s county fair – a suburban Farmer’s market in south-west London. We didn’t have an ox to spare, so in our case the crowd had to correctly guess the number of chocolate Easter eggs to win the prize (see below, we’ll skate over the health effects of eating all of those eggs…).<o:p></o:p></div><div class="MsoNormal"><br /></div><div class="separator" style="clear: both; text-align: center;"><a href="https://4.bp.blogspot.com/-IZg2D08Zbpw/WrDAICpkxCI/AAAAAAAAA2M/FBjqrZFN5OE1DrIbRuoxDJLjfcnLQsXHQCLcBGAs/s1600/20180315_191725.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" data-original-height="800" data-original-width="450" height="320" src="https://4.bp.blogspot.com/-IZg2D08Zbpw/WrDAICpkxCI/AAAAAAAAA2M/FBjqrZFN5OE1DrIbRuoxDJLjfcnLQsXHQCLcBGAs/s320/20180315_191725.jpg" width="180" /></a></div><div class="MsoNormal"><br /></div><div class="MsoNormal"><br /></div><div class="MsoNormal">This was my chance to get my hands on a real world data set. Unfortunately the weekend coincided with a blizzard, so turn-out was low at the market and I was worried that the dataset wouldn’t be sufficient to show the effect. In the end we had 66 entries – and the correct answer was 145 eggs. The answers were all over the place, with a low of 50 and a maximum of 376 (see scatter chart below – correct answer in red). The lucky winner got close with an answer of 143. <o:p></o:p></div><div class="MsoNormal"><br /></div><div class="separator" style="clear: both; text-align: center;"><a href="https://2.bp.blogspot.com/-U8dsarUmhzg/WrDAmbKyisI/AAAAAAAAA2Q/B5f6TnL6Zn8aEirEalpKspVejaPoO_H7gCLcBGAs/s1600/eggs-scatter.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" data-original-height="289" data-original-width="621" height="148" src="https://2.bp.blogspot.com/-U8dsarUmhzg/WrDAmbKyisI/AAAAAAAAA2Q/B5f6TnL6Zn8aEirEalpKspVejaPoO_H7gCLcBGAs/s320/eggs-scatter.png" width="320" /></a></div><div class="MsoNormal"><br /></div><div class="MsoNormal"><br /></div><div class="MsoNormal">So how wise was our crowd of 66? The average of the entire data set was 144.1 – which is closer than the winning entry. I have to admit I was surprised at just how close that is. Even more surprising is how quickly the average converged to the correct answer. The chart below shows the cumulative moving average converging close to the right answer within 15 guesses. That’s fast.<o:p></o:p></div><div class="MsoNormal"><br /></div><div class="separator" style="clear: both; text-align: center;"><a href="https://2.bp.blogspot.com/-cbnL5a33jQQ/WrDA4qTjvpI/AAAAAAAAA2Y/pnPq9dW2b1YEkltxzY7sLJgab9oe6gFPACLcBGAs/s1600/eggs-cma-forward.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" data-original-height="327" data-original-width="621" height="168" src="https://2.bp.blogspot.com/-cbnL5a33jQQ/WrDA4qTjvpI/AAAAAAAAA2Y/pnPq9dW2b1YEkltxzY7sLJgab9oe6gFPACLcBGAs/s320/eggs-cma-forward.png" width="320" /></a></div><div class="MsoNormal"><br /></div><div class="MsoNormal">Was that speed of convergence just a fluke? When the dataset is reversed what happens? The same thing – the cumulative moving average gets close to the correct average incredibly quickly, even though it starts off with some wildcard answers.<o:p></o:p></div><div class="MsoNormal"><br /></div><div class="separator" style="clear: both; text-align: center;"><a href="https://3.bp.blogspot.com/-74O7LHjaQF8/WrDBtKcjXdI/AAAAAAAAA2o/QuIb9XDqdGwV1xsMvZxluIIvNNI5WkAPgCEwYBhgL/s1600/eggs-cma-reverse.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" data-original-height="327" data-original-width="621" height="168" src="https://3.bp.blogspot.com/-74O7LHjaQF8/WrDBtKcjXdI/AAAAAAAAA2o/QuIb9XDqdGwV1xsMvZxluIIvNNI5WkAPgCEwYBhgL/s320/eggs-cma-reverse.png" width="320" /></a></div><div class="MsoNormal"><br /></div><div class="MsoNormal">Although this idea might be old hat – I for one am still impressed at these results. Although the applications for this idea are limited – it would be great to be able to harness this sort of thing to solve something a bit more meaningful than the size of an ox or the number of chocolate eggs. I also find the democratic nature of this result incredibly satisfying.<o:p></o:p></div><br /></div>Pan Pantziarkanoreply@blogger.com0tag:blogger.com,1999:blog-4826023149139426251.post-12085061543983179322017-04-26T07:54:00.001+01:002017-04-26T07:54:43.519+01:00Myc, Models and Tumour Growth<div dir="ltr" style="text-align: left;" trbidi="on"><div>When I wrote the NEATG model of tumour growth, published in the journal PeerJ (<a href="https://peerj.com/articles/2176/">https://peerj.com/articles/2176/</a>), I focused on the behaviour of individual cells and on the role of cell competition and cell death in tumour growth. All models have to simplify and abstract, and the NEATG model does exactly that. The model steered clear of the molecular basis for the behaviour of the cells – my working assumption was that cells produce soluble factors and signalling proteins that mediate their cell-cell and cell-tissue interactions. It was one of the reasons I called the model NEATG (<i>Non-physiological</i> Evolutionary Algorithm for Tumour Growth – though as <a href="http://benzekry.perso.math.cnrs.fr/" target="_blank">Sebastien Benzekry</a> pointed out to me, the fact that the model has cells and tissues already makes it fairly physiological… ).</div><br /><div>Despite the level of abstraction, the model clearly does show cellular behaviours that mimic aspects of tumour growth and response to cytotoxic chemotherapy.&nbsp; A surprise for me was that the model showed that accelerated tumour regrowth following chemotherapy is driven by cell competition and the levels of cell death. I spent time looking at the research literature on these topics and found that my results were actually in line with clinically relevant phenomena – which is what makes the model interesting.</div><br /><div>A recent paper from a group of researchers from the University of Bologna entitled <i><a href="http://www.mdpi.com/2073-4425/8/4/120/htm" target="_blank">MYC, CellCompetition, and Cell Death in Cancer: The Inseparable Triad</a> </i>&nbsp;(available open access from the journal genes – it’s well worth a read), casts some interesting light on the topic. C-Myc is one of the most important of the master genes involved in cell cycle progression and tissue growth. It’s a transcription factor, which means it regulates the activity of other genes, and is often switched on permanently in tumours rather than coming on and off as required. It’s widely associated with a whole range of different cancers.</div><br /><div>In this paper the authors review recent evidence from <i>Drosophilia</i> (fruit fly) models of cancer and how they are implicated in cell growth, cell death and cell competition. They outline the way that competition selects for cells that are ‘fittest’ and that less fit cells are effectively killed off – in just the way that they do in software in my model. The evidence that they outline suggests that one of the drivers for the behaviour of these cells is c-Myc, making it an important component at the physiological level missing from NEATG.The authors themselves make note of the results from the NEATG model:</div><br /><div><i>Our findings suggest that CC [cell competition] is an innate process governing both cancer initiation and progression, where cell death fuels the clonal expansion of the fittest cells in the context. CC and apoptosis thus appear to be strictly linked one another, and emerge as fundamental cancer drivers also in a computational model of tumour growth, where several parameters of malignancy such as intra-tumour heterogeneity and accelerated repopulation have been taken into account.</i></div><br /><div>For the next stage of work on this model I will be investigating the metabolic impact of cell growth in tumour growth, and the impact that cell death has on this. My prediction is that the model will show that populations of ‘super-feeders’ will emerge during tumour growth – and that chemotherapy helps to select for these populations of cells. However, as this stage I don’t really know that that’s what happens – I have to wait and see what the data tells me…</div><br /><div>In the meantime I’ll finish with some final words from the team at Bologna :</div><br /><div><i>Cells cooperate to build an organ and, in a similar way, they cooperate to build a cancer. Although the contexts are impressively distant, MYC-mediated cell competition seems to be at work in both cases with the same basic, sequential elements: cell–cell disparity in MYC contents, death of the cells with lower MYC levels, and proliferation of the cells with higher MYC levels. This stereotypical module shapes organ development and, possibly, cancer evolution. In growing tumours, an excess of dying cells is known to contribute to mass expansion, but the implication of MYC-mediated cell competition in this cancer trait has just begun to be investigated. Further research is warranted on the intricate “life and death” signals exchanged by confronting cell populations within the cancer community.</i><br /><br /><br /></div></div>Pan Pantziarkanoreply@blogger.com0tag:blogger.com,1999:blog-4826023149139426251.post-7661925704381504882017-02-22T07:56:00.000+00:002017-02-22T07:56:04.987+00:00The Star Throwers Guide To Cancer<div dir="ltr" style="text-align: left;" trbidi="on">One of the reasons for starting this website was the wish to share information with patients, carers and other people directly affected by a cancer diagnosis. The site came out of a series of discussions I had with my <a href="http://www.anticancer.org.uk/p/about.html">son George</a> while he was in the middle of his battle against osteosarcoma. We wanted a site that could be used to share science-based information that was likely to be useful, particularly for people looking for treatment options, as we often were. However, &nbsp;I have to admit that in recent months the site hasn’t been getting the attention it used to – the number of new postings has been really light on the ground. One of the reasons for this has been that for a long time I had been working with the UK charity <a href="http://www.starthrowers.org.uk/">Star Throwers</a> to produce a book that would provide a lot of that type of information in ebook and paperback form.<br /><br /><a href="http://newparadigmpublishing.co.uk/star-throwers-guide-to-cancer/">The Star Thowers Guide To Cancer</a>, as the book is called, is now available via Amazon or, if you’re in Wymondham, Norfolk, direct from Star Throwers. The book covers similar ground to this website: science-based, heavy on information, concise and geared very much to looking at new treatment options. Does the world really need another new book on cancer? Book shops are full of new cancer books: memoirs, diet guides, histories of oncology and much more. But this one is different.<br /><br /><a href="https://www.amazon.co.uk/Star-Throwers-Guide-Cancer-depth/dp/1537419250/454" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;" target="_blank"><img border="0" height="320" src="https://1.bp.blogspot.com/-Ob4uvSpox-s/WK1C2_bL7YI/AAAAAAAAAnE/zOHdb5up7Tct3ARd09Oa9zggVl58pQHoACLcB/s320/front.PNG" width="208" /></a>I like to think of this book as a ‘how to be a difficult patient’ guide. It shows you how to read the cancer literature. How to assess the breathless stories about new ‘cures’ that are frequently highlighted in the mass media. There is a detailed discussion of the tricky subject of cancer and diet. Searching for clinical trials and looking for treatments abroad are also covered in some detail. Local ablative treatments such as cryoablation are covered, including the vital information on where to look for these useful but underused treatments. Finally, there is also a chapter on <a href="http://www.anticancer.org.uk/search/label/repurposing">drug repurposing</a>, a topic I have covered here many times and which I now work on pretty much full-time.<br /><br />In the past I have considered taking the best articles from this site and putting them together as a single download via PDF. But there’s no need now. This book provides the best of this site and much, much more.<br /><div><br /></div></div>Pan Pantziarkanoreply@blogger.com0tag:blogger.com,1999:blog-4826023149139426251.post-29962227006943705802016-12-06T21:27:00.004+00:002016-12-06T21:27:46.939+00:00Aspirin as an anti-metastatic drug - in 1977<div dir="ltr" style="text-align: left;" trbidi="on">Working on drug repurposing often involves an element of historical research. Drugs like <a href="http://www.anticancer.org.uk/2014/11/cimetidine-as-anticancer-drug-new-redo.html">cimetidine</a>, <a href="http://www.anticancer.org.uk/2015/09/the-latest-redo-paper-nitroglycerin.html">nitroglycerin</a> and <a href="http://www.anticancerfund.org/news/pers-release-its-time-to-consider-propranolol-as-an-anti-cancer-drug-researchers-say">propranolol </a>have been around for decades and there’s a lot of good data that we can extract from old articles, clinical trials and retrospective studies. One of the best known examples of old drugs is aspirin - which is attracting a huge amount of attention from clinical researchers in oncology. There is a huge literature on aspirin, with much more on the way as clinical trials are designed, run and reported.<br /><br />One of the most intriguing things about aspirin is the data that suggests that it might work as an anti-metastatic agent. There is data that shows that aspirin may be effective in reducing the risk of metastatic spread in breast, prostate and colon cancer (for example this <a href="http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0152402">recent meta-analysis</a> reported a relative risk of metastasis of 0.77 with aspirin).<br /><br />That we’ve known about the anti-cancer potential of aspirin for a long time isn’t a surprise – but I have to admit to being surprised to come across a paper from 1977 arguing the case that aspirin might be an effective anti-metastatic drug. The paper is <b>Aspirin for reducing cancer metastases?</b> by Henschke, Luande and Choppala (J Natl Med Assoc. 1977 Aug;69(8):581-4). The paper is available open access (<a href="https://www.ncbi.nlm.nih.gov/pubmed/904011">here</a>), and while the data is old, the arguments it makes are still vital and relevant. It really begs the question, how is that things haven’t moved forward more quickly? And, more crucially, how can we make sure that things move forward more quickly in the future. Not just for aspirin but for so many of the other old drugs that have good data in their favour. <br /><br /></div>Pan Pantziarkanoreply@blogger.com0tag:blogger.com,1999:blog-4826023149139426251.post-80778137826306381252016-11-23T14:54:00.000+00:002016-11-23T14:54:15.918+00:00Innovative new brain tumour trial kicks off<div dir="ltr" style="text-align: left;" trbidi="on">The Anticancer Fund is pleased to announce that on Tuesday 15th November 2016, the first patient was enrolled in a clinical trial called CUSP9v3 for recurrent glioblastoma at the Department of Neurosurgery, University Hospital of Ulm, Germany. This is a phase 1 clinical trial. The study treatment will be given to 10 patients to assess safety and tolerability.<br /><br />Glioblastoma is the most frequent type of malignant brain tumour in adults. In Europe and North America, there are 3-4 new cases per 100,000 inhabitants per year. Even when all visible tumour is surgically removed, glioblastoma almost always returns within a year. Therefore, after surgery patients are treated with radiotherapy and chemotherapy. Despite this additional treatment, glioblastomas usually regrow and at some point can no longer be effectively treated, often resulting in death 1-2 years after the initial diagnosis.<br /><br />&nbsp;"For decades, researchers have been looking for new experimental therapies for our patients with no real success yet" says Professor Marc-Eric Halatsch, the neurosurgeon leading the trial. "Together with Dr Richard Kast (USA), we sought to address the problem that glioblastomas usually find a way to escape the action of a single drug. In 2013, we teamed up with an international group of researchers to propose a treatment that would act on multiple mechanisms used by glioblastoma cells to grow. This treatment consists of 9 drugs that are currently on the market for other indications than cancer (‘repurposed’ drugs). These nine drugs have ancillary attributes that block several of the mechanisms glioblastoma cells use to grow. These drugs had remarkable effects in preventing growth of glioblastoma cells in preclinical studies. A clinical trial was warranted."<br /><br />In addition to contributing to the design and set-up of the trial, the Anticancer Fund will provide €300,000 for this study. "This type of treatment is not developed by the pharma industry because the 9 drugs are from different companies and all are off-patent and mostly available as generics" says Lydie Meheus, director of the Anticancer Fund. "This implies that the treatment, if successful, will not generate substantial additional financial return for the manufacturers of the drugs. Since the treatment can benefit patients and the healthcare system, it must be developed with the support of philanthropy and governments."<br /><br />Patients participating in the trial will receive CUSP9v3 for one year. When all patients have completed 2 months of treatment, a first analysis will be done on the safety and tolerability of the combined treatment.<br /><br />If the combination is well tolerated, a larger multi-centre study will be initiated to evaluate the treatment’s efficacy.<br /><br />Further information on the CUSP9v3 trial can be found on <a href="http://www.anticancerfund.org/">www.anticancerfund.org</a> or on www.clinicaltrials.gov (NCT02770378).<br /><div><br /></div></div>Pan Pantziarkanoreply@blogger.com0tag:blogger.com,1999:blog-4826023149139426251.post-7784474857145359312016-06-22T07:49:00.000+01:002016-06-25T11:19:26.500+01:00Guest Post - Crowdfunding for Pediatric Cancers<div dir="ltr" style="text-align: left;" trbidi="on">Cesare Spadoni, founder of aPODD (accelerate Paediatric Oncology Drug Development), talks to Pan Pantziarka about the problems in drug development in children&#39;s cancers, and about the <a href="https://www.futsci.com/project/child-brain-cancer" target="_blank">crowdfunding campaign</a> to find a new treatment for Medulloblastoma.<br><br><b>Pan: </b>What is the aPODD foundation aiming to do?<br><b>Cesare</b>: aPODD (accelerate Paediatric Oncology Drug Development) was set up with the mission to speed up the development of better and safer treatments for children with cancer. This is a cause that is very close to my heart. I lost my first daughter to cancer a few years ago. That is when I began thinking about doing something for children with cancer.<br><br>Obviously, you can have a positive impact on sick children and their families in many different ways. In my case, because of my professional background in drug development, I felt compelled to do something to address the major problem preventing any further clinical improvement for children and adolescents with cancer: the lack of therapeutic options and the delayed access to the most innovative treatments.<br><br>Specific anti-cancer drugs are not developed for younger patients because it is not profitable for industry to do so. This is an area where patients’ organisations may play a vital role. Drug repurposing is certainly an area we are very much interested in. By looking at existing drugs we may be in a position to identify possible new treatments much faster and at a fraction of the cost and risk of new drug development<br><br><b>Pan</b>: How is this campaign different to others?<br><b>Cesare</b>: We are looking to identify a potential new treatment for Medulloblastoma, a rather aggressive form of brain cancer that is more frequent in children and adolescents. The current therapeutic options for this cancer are limited and very harsh, including high dose chemotherapy and radiotherapy. The impact on patients may be devastating as the lucky survivors may face severe health problems later in life.<br><br>For this project we are partnering with Healx, a company based in Cambridge (UK), which offers very advanced technologies and strong expertise in drug re-purposing. Healx is applying advanced computational biology tools, data analytics and machine learning to make sense of complex biological data sets and match those with the profiles of known drugs.<br><br>We are now in the process of finalising a list of drugs that we would like to test experimentally in Medulloblastoma cell lines in view of progressing further with the most promising ones.<br>We are very excited by these early results and we are really hope that this crowdfunding is successful so that we can proceed as fast as we can.<br><br></div><a href="http://www.anticancer.org.uk/2016/06/guest-post-crowdfunding-for-pediatric.html#more">Read more »</a>Pan Pantziarkanoreply@blogger.com0tag:blogger.com,1999:blog-4826023149139426251.post-12014323684800907132015-12-14T20:53:00.000+00:002017-04-26T07:54:58.780+01:00NEATG - A software model of cancer<div dir="ltr" style="text-align: left;" trbidi="on">For a huge chunk of my working life I have built computer models which were used to assess operational activities in different industries. The combination of mathematics and software can provide enormous power to help understand and assess complex processes. My doctorate put these skills to good use in that I used software implementations of evolutionary processes to build a system that evolved mathematical models which could validate the correctness, or otherwise, of large data sets. In plain English I used genetic algorithms to discover mathematical models which could pick out incorrect data values in large volumes of data. Think of a system that could take the largest Excel spreadsheets and automatically flag those rows of data which were most likely to be in error – all without knowing what the spreadsheet data represented or who had put it together or why.<br /><br />Of course cancer is the ultimate in evolutionary systems – if you wanted to design a system to illustrate the evolution at work you’d come up with something pretty much like it. When we look at cancer and see that some treatments have fantastic initial responses, with tumours shrinking away to almost nothing, followed by a rebound in which the cancer comes back more aggressive and resistant to the treatment then we’re seeing evolution at work.<br /><br />Given my background in computer modelling and my current work in oncology it should be no surprise that I’ve worked on a software model of tumour growth. I’ve called it NEATG – for Non-physiological Evolutionary Algorithm for Tumour Growth. It’s a computational model – it’s about algorithms rather than about trying to recreate in software the vast complexities and details of cells, proteins, signals and pathways. Although it’s a simple model by design, it does illustrate some interesting behaviour that brings to mind the behaviour of real tumour growth.<br /><br /><table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody><tr><td style="text-align: center;"><a href="http://1.bp.blogspot.com/-cE2GROWf4Ok/Vm8sFo82oaI/AAAAAAAAAYI/3W9mslZecOY/s1600/NEATG%2Bgraphics.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="166" src="https://1.bp.blogspot.com/-cE2GROWf4Ok/Vm8sFo82oaI/AAAAAAAAAYI/3W9mslZecOY/s400/NEATG%2Bgraphics.png" width="400" /></a></td></tr><tr><td class="tr-caption" style="text-align: center;">Tumour growth in NEATG</td></tr></tbody></table><br />For example, the NEATG system can model the growth of a tumour mass (in two dimensions), it can model the rise of genetically different sub-populations of cancer cells, and it can model different interventions such as chemotherapy or nutrient deprivation. What is more it displays emergent behaviour – such as a more aggressive growth pattern following the cessation of treatment. This is behaviour that emerges naturally from the interactions between cells and tissues, not behaviour that has been explicitly programmed into the system as a set of predefined rules.<br /><br />For now NEATG is a tool that can be used to explore different algorithmic scenarios – you can play try out different thought experiments to see what happens. It’s good for thinking about some of the most fundamental aspects of cancer without getting bogged down in the molecular biology. For example, while most people think of cancer as primarily a disease of disordered genes – a view known as the ‘somatic mutation theory’ of cancer – there is an alternative theory called the ‘tissue organisation field theory’ of cancer. In this theory disordered genes are more of a by-product than a cause of cancer, and it places more emphasis at the disordered tissue environment. Simplistically we can ask: is it the delinquent cell or the bad neighbourhood that causes cancer? This is a good question to explore using a suitable software model – and I hope that NEATG can be applied to this.<br /><br />While it’s still early days for this piece of work, I have written a paper on it which is available as a preprint (i.e. prior to peer review) at <a href="https://peerj.com/preprints/1558/">PeerJ</a>. If you’re interested please take a look. <br /><br /></div>Pan Pantziarkanoreply@blogger.com0tag:blogger.com,1999:blog-4826023149139426251.post-5425528056752605022015-11-09T21:21:00.001+00:002015-11-09T21:21:56.519+00:00Kick-starting the immune systemOne of the hottest topics in oncology right now is the use of the latest generation of immunotherapy drugs, particularly drugs called checkpoint inhibitors – also known as anti-PD1/PDl1 and anti-CTLA4 drugs. The most well-known of these are ipilimumab (Yervoy), pembrolizumab (Keytruda), and nivolumab (Opdivo) – drugs which are making headlines the world over with some truly astonishing instances of remission in metastatic melanoma and other hard to treat cancers. However, as with many other targeted therapies, there are also two major problems with these treatments. The first is that only a subset of patients show any response, and sometimes these responses do not last for very long before resistance kicks in. A second problem is that these drugs are not without side effects, some of them quite serious. It’s this first problem that I want to focus on in this blog post.<br /><br />Being able to improve the response rate to these treatments would mean that many more advanced cancer patients may benefit from these treatments. This is an area of intense research at the moment, with multiple trials looking at different mechanisms to address the issue. One obvious response has been to investigate combination treatments in which two of these drugs are used together – for example ipilimumab and nivolumab together. Results so far suggest that the combination is effective, with a major Phase III clinical trial in untreated metastatic melanoma showing longer median progression free survival for the combination compared to either treatment alone.<br /><br />Another approach is to combine checkpoint inhibitors with radiotherapy or chemotherapy. The idea here is to use existing treatments to cause tumour cell death and in the process cause an immune response that the checkpoint inhibitors then amplify in some way. It’s an appealing approach but it does depend on using treatments that are ‘immunogenic’ that is they cause an immune response to develop. One of the recurring problems in cancer treatment is the emergence of immune suppression or skewing of the response to pro-tumour responses. Evidence is emerging that a lack of an anti-tumour response is related to the lack of response to the checkpoint inhibitors in some patients.<br /><br />All of which brings us to consider whether there is a role for some safe and non-toxic treatments which can aid in reversing this cancer-associated immune suppression. Are there ways in which we can kickstart the immune response in ways which synergise with these checkpoint inhibitors?<br /><br />A number of possibilities spring to mind using some well-known repurposed drugs. The first is cimetidine (Tagamet), one of the first of the blockbuster antacid drugs and with well-documented anti-cancer activities (summarised in the ReDO paper <a href="http://ecancer.org/journal/8/485-repurposing-drugs-in-oncology-redo-cimetidine-as-an-anti-cancer-agent.php">here</a>). Cimetidine has been shown to cause an increase in the number of tumour-infiltrating lymphocytes and to deplete T-reg and MDSC immune-suppressing cells. This makes it an interesting candidate to explore in cancer even without checkpoint inhibitors, but the combination with checkpoint inhibitors would be especially interesting.<br /><br />Another possibility is to use some non-steroidal anti-inflammatory drugs which have also been shown to have positive effects in cancer immunity. And it’s not just COX-2 inhibitors like celecoxib which are interesting here, there is evidence that diclofenac, which inhibits both COX-1 and COX-2 may have positive effects via its action on the PGE2/IDO pathway. It may well be that the positive effects that have been shown by <a href="http://www.anticancer.org.uk/2013/09/ketorolac-and-breast-cancer.html">ketorolac in reducing breast cancer recurrence</a> rates – now the subject of a study in Belgium – are partly immune related.<br /><br />Finally, there is also the possibility that gut bacteria may have a role. This is a topic I have written about in the past – it is increasingly clear that our <a href="http://www.anticancer.org.uk/2014/01/probiotics-and-cancer-risk.html">gut bacteria have a systemic impact</a> on our immune system. This should be no surprise when you think about it – as a race we have evolved complex relationships with our bacteria, they are more than just along for the ride and are integral to digestion and &nbsp;immunity alike. A <a href="http://www.ncbi.nlm.nih.gov/pubmed/26541606">recent paper</a> published in the journal Science explored the role of gut bacteria in mice and the different rates of melanoma growth in two different sets of mice. These mice were of the same species but differed in their gut bacteria – and interestingly the tumour growth rates were markedly different.<br /><br />Putting these two sets of mice into shared cages, so that they cross-colonised each other with their bacteria, abolished the different growth rates. The mice with the faster tumour growth rate now had slower tumour growth rates than the mice with the slower rate. This was further tested by taking the ‘fast’ mice and explicitly transferring bacteria from the ‘slow’ mice into them – with the same outcome. Finally, adding these bacteria to treatment with a checkpoint inhibitor almost abolished the tumour growth. This is a fairly stunning result – it suggests that changing the gut bacteria can make a significant difference to immunotherapy with the latest drugs. And, for those who are interested, the bacteria were from the <i>Bifidobacterium</i> family – often used in live yoghurt.<br /><br />Allowing the immune system to mount an effective anti-tumour response is almost a holy grail in oncology – perhaps we are finally coming to the point where we can look at a using combination therapies which work together to do exactly that.<br /><br />Pan Pantziarkanoreply@blogger.com0tag:blogger.com,1999:blog-4826023149139426251.post-18792618798119062602015-10-06T20:44:00.000+01:002015-10-06T20:44:07.326+01:00Crowdfunding Against CancerOne of the many problems associated with <a href="http://www.redo-project.org/">repurposing</a> off-patent drugs for new uses in cancer is that there is no commercial sponsor involved in the process of getting the drug into clinical use. On the face of it this might seem like a good thing – surely it means that there will be nobody jacking the price up to make huge profits from previously cheap drugs. But in practice this means that the very expensive process of gaining evidence of efficacy in clinical trials though to applying for a new licence is hamstrung due to lack of funding. Clinical trials, especially the larger pivotal trials which convince clinicians that a treatment is effective, are expensive to design and run. For a new drug anywhere up to 75% of the billion dollar cost of getting it to market is spent on the trials process.<br /><br />This is a significant problem but not an insurmountable one. The <a href="http://www.anticancerfund.org/">Anticancer Fund</a>, for example, is funding a number of clinical trials using a range of repurposed drugs – for example a trial of the pain-killer <a href="http://www.anticancerfund.org/projects/ketorolac-in-breast-cancer-surgery">ketorolac in breast cancer</a>, or a mix of drugs in <a href="http://www.anticancerfund.org/projects/metzolimos-a-combination-of-4-repurposed-drugs-studied-in-patients-with-advanced-solid-tumo">recurrent osteosarcoma</a>. Another notable example is the <a href="http://www.addaspirintrial.org/">Add-Aspirin</a> trial, which is part funded by Cancer Research UK. Clearly there is a role for the not-for-profit sector to step in – but is there also a role for a more direct role for the public?<br /><br />The Neo-Art trial is looking at using the generic drug artesunate – a commonly used ant-malarial drug – as a treatment in colorectal cancer. Like the ketorolac in breast cancer trial, this one is looking to reduce the rate of post-surgical relapse. Remember, it’s most often metastatic disease which kills cancer patients. Any intervention which can stop metastatic disease in its tracks can have huge impact on overall survival. This is an idea which we urgently need to explore in a range of cancers, including osteosarcoma, as I have <a href="http://www.anticancer.org.uk/2014/06/osteosarcoma-proposal-for-reducing.html">suggested in the past</a>.<br /><br />In the case of the <a href="https://futsci.com/project/antimalarial-cancer">Neo-Art trial</a>, the team at St George’s Hospital have already got preliminary data in patients suggesting that two weeks of artesunate prior to surgery can have a major impact on the relapse rate. The new trial is aiming to prove that this is the case in a larger population of patients – 140 in all. Much of the funding for the trial is coming from a small charity called <a href="http://boweldisease.org.uk/">Bowel Diseases UK</a>, but there’s an additional £50,000 required – and this is where the public can have a direct role.<br /><br />In a pioneering move, the St George’s team are working with a crowdfunding platform called FutSci to appeal directly to patients, families and members of the public to raise the funds required to make the trial happen. So far the results have been impressive and the appeal is nearly 70% of the way there – but that still leaves around £15,000 to be raised. So, if you have ever been touched by bowel cancer, or want to be part of something that could be truly groundbreaking - &nbsp;then please go ahead and make a <a href="https://futsci.com/project/antimalarial-cancer">donation</a>.<br /><div><br /></div>Pan Pantziarkanoreply@blogger.com0tag:blogger.com,1999:blog-4826023149139426251.post-34350628921776682522015-09-18T08:01:00.000+01:002015-09-18T08:01:11.819+01:00The latest ReDO paper - nitroglycerinA long while back I blogged about the possible anticancer uses of <a href="http://www.anticancer.org.uk/2014/09/nitroglycerin-and-cancer-drug-therapy.html">nitroglycerin</a>&nbsp; - a drug with a history of use going back 125 years or more. This was also the topic of our most recently published paper in the journal ecancer series from the <a href="http://www.redo-project.org/">Repurposing Drugs in Oncology project</a>.<br /><br />Talking of repurposing - a topic which is gaining interest all the time - there are some new developments in the Off-patent Drugs Bill which I will blog about at a later point. This offers a legislative solution to the problem of licensing an old drug for a new disease - an essential step that has to be taken if we are serious about changing medical practice. More on that later. <br /><br />Pan Pantziarkanoreply@blogger.com0tag:blogger.com,1999:blog-4826023149139426251.post-40794569672400893682015-05-28T09:25:00.001+01:002015-05-28T09:25:18.889+01:00LFS - Primed for cancer - InterviewThe excellent <b><i>Living LFS</i></b> blog has a new piece which covers my latest &nbsp;paper on Li Fraumeni Syndrome...<br /><br /><a href="http://livinglfs.blogspot.co.uk/2015/05/primed-for-cancer-with-pan-pantziarka.html">http://livinglfs.blogspot.co.uk/2015/05/primed-for-cancer-with-pan-pantziarka.html</a><br /><br />This explains the core details of the paper in very non-technical language and explains what it may mean in practice. So, if the technical nature of the original paper gets in the way, then this is certainly a good alternative.<br /><br />Pan Pantziarkanoreply@blogger.com0tag:blogger.com,1999:blog-4826023149139426251.post-61659618171911558772015-05-22T07:40:00.003+01:002015-05-22T07:40:29.262+01:00Press release - Primed for cancer?Li Fraumeni Syndrome (LFS), a rare genetic condition that predisposes sufferers to cancer development, is associated with mutations in the TP53 tumour suppressor gene. Although rare, LFS sufferers have a highly elevated risk of developing one or more cancers, with some estimates putting the life-time risk at 70% for males and 100% for females. However, new research published today in leading online oncology journal ecancermedicalscience, suggests that cancer development may be due to more than a mutated tumour suppressor function. <br /><br />In a new paper by Pan Pantziarka PhD, a scientist working for the Anticancer Fund and co-ordinator of the <a href="http://www.redo-project.org/">Repurposing Drugs in Oncology(ReDO) project</a>, it is suggested that there are other important functions of the TP53 gene that contribute to this elevated cancer risk. 'Our knowledge of the multi-faceted functions of TP53 has grown enormously in the last few years,' Pantziarka says, 'yet much of this new information has yet to be integrated into our understanding of the disease process in people with LFS'. <br /><br />Sue Armstrong, author of 'p53: The Gene that Cracked the Cancer Code', points out that: 'TP53 is the most commonly mutated gene in human cancer. Indeed it’s probably fair to say that if this key tumour suppressor is functioning properly, it’s almost impossible for cancer to develop. It follows that to be born with mutant - and therefore malfunctioning - TP53 in every cell in the body is to be extremely vulnerable to cancer. This is the tragic fate of people with Li Fraumeni Syndrome, for whom conventional therapies rarely offer more than temporary respite. So, new ways of looking at, and treating, cancer are sorely needed.' <br /><br />Known as the 'guardian of the genome', the p53 protein is at the heart of an array of signalling networks involved in responding to DNA damage, metabolic stress, immunity, senescence and ageing. In people with normal p53 function, the kinds of damage that cause cells to become cancerous trigger a damage response that normally leads to the cell self-destructing before it can proliferate, a process called apoptosis. But in people born with a mutated TP53 gene this process does not take place. However, there is more to cancer than delinquent cells, increasingly we understand that cancer also involves a supporting micro-environment to provide a blood supply, nutrients, protection from an immune response and so on. These factors may also involve p53, and Pantziarka's hypothesis suggests that people with LFS are born 'primed for cancer' because many of these cancer-support systems are already in place thanks to the mutation. <br /><br />Pantziarka has first-hand knowledge of this disease process himself, having lost his first wife and his teenage son, George, to cancers due to LFS. George, for example, developed his first cancer at the age of two and subsequently developed two further primary cancers before succumbing to metastatic sarcoma in 2011. The story is told in a recent book, 'For The Love of George' by Irene Kappes, available from Amazon and other booksellers. The family have also established the George Pantziarka TP53 Trust (www.tp53.org.uk) to provide support for other families and to promote research into the condition. <br /><br />This new hypothesis does more than provide a more nuanced view of cancer development in people with LFS, it also suggests that many of these additional factors may be amenable to drug treatment. 'By expanding our view of carcinogenesis in LFS we may also be broadening the range of interventions available to us to change things. The key thing,' Pantziarka underlines, 'is to start looking at active measures we can take to reduce this risk. Drugs such as metformin may hold the promise of reducing that life-time risk by some significant margin.' <br /><br />In perhaps the most radical section of the paper, it is suggested that some other cancer predisposition syndromes, caused by mutations in other genes, may share some of the same features of LFS despite the different genetic drivers. If this is the case, as the paper suggests, then perhaps some of the active measures which warrant investigation in LFS may also apply to a range of different genetic cancer predisposition syndromes. In such a case the prospect of a clinical trial that targets multiple high-risk patient populations is an alluring prospect. 'With limited population sizes it is difficult to design cancer-prevention trials because the sample sizes are too low,' Pantziarka explains, 'but if my theory is correct then we can pool different populations into the same trial and look for reduced cancer incidence across the board.' <br /><br />=============================================<br />Links/Contacts:<br />The George Pantziarka TP53 Trust – <a href="http://www.tp53.org.uk/">www.tp53.org.uk</a><br />Original paper (publication date 21/05/15): ‘Primed for cancer: Li Fraumeni Syndrome and the pre-cancerous niche’ -<a href="http://ecancer.org/journal/9/541-primed-for-cancer-li-fraumeni-syndrome-and-the-pre-cancerous-niche.php" target="_blank">http://ecancer.org/journal/9/541-primed-for-cancer-li-fraumeni-syndrome-and-the-pre-cancerous-niche.php </a>Pan Pantziarkanoreply@blogger.com0tag:blogger.com,1999:blog-4826023149139426251.post-50143035168723717542015-03-18T21:33:00.000+00:002015-03-18T21:33:02.680+00:00Exercise and Breast CancerI was alerted today to an interesting new paper in the Journal of the National Cancer Institute that looked at the effect of exercise on tumour blood supply and the response to chemotherapy in breast cancer. Now this is a topic which is worth paying attention to – there is lots of evidence that daily exercise can reduce breast cancer recurrence, have positive effects on physical status and may even improve overall survival in women with breast cancer. With that in mind, what does this <a href="http://jnci.oxfordjournals.org/content/107/5/djv040.full">new paper</a>&nbsp;tell us?<br /><br />Firstly, it’s important to note that this isn’t a study in people – this is a study in mice. But these are mice with intact immune systems and they are bearing mouse tumours. It means that although this is an animal model we can trust the evidence a bit more than we can when dealing with immune deficient mice implanted with human tumours. Secondly we should note that these mice were not forced to do exercise – so there was no additional stress involved and there were no enforced amounts of exercise that had to be performed. Basically the mice were given an environment which gave them an exercise wheel they could use, whereas the comparison group didn’t have the opportunity to exercise. Finally, some of the mice had ER+ and some ER- tumours, matching human tumours in hormone responsive and non-responsive sub-types.<br /><br />What the study showed was that the mice doing the exercise had a reduced the tumour growth rate, an increased the rate of cancer cell death (apoptosis), increased the maturity of the tumour blood vessels, increased tumour blood flow and reduced the areas that were starved of oxygen (hypoxia). These are all things which are positive and which we definitely would want to achieve clinically. Basically these results show that exercise normalises the tumour blood supply. This is a good thing.<br /><br />Normally the tumour blood supply is chaotic – vessels are immature, leaky, misconnected. This chaotic blood supply has a number of downsides. Firstly it means that the drugs we give cancer patients to kill the tumour often don’t make it into the interior of the tumour – not good because if they don’t in they won’t work. Secondly the chaos causes areas of the tumour to become starved of oxygen and nutrients – this in turn causes the cancer cells to become more aggressive and dangerous as they adapt to these harsh conditions.<br /><br />So, normalising the blood supply means that tumours are not forced to become more aggressive and, as we see in these results, this can lead to a slower growth rate. It also means that when drugs are administered they can make it into a greater portion of the tumour. And this is where the second lot of results come in. Mice treated with the chemotherapy drug cyclophosphamide had greater response if they were exercising compared to the sedentary mice. Interestingly, mice who did exercise alone (no chemo) showed a similar response to mice treated with chemo alone. But the best response came from mice who had chemo and did exercise.<br /><br />These are positive results but we do have to keep in mind that this is in mice. However, it backs up what we know from evidence in humans and suggests reasons for why we’ve seen these results. The take home from this is that exercise has a positive effect in breast cancer – and most likely in other cancers too. It doesn’t have to be running a marathon every week either – <a href="http://jama.jamanetwork.com/article.aspx?articleid=200955">a study in women with breast cancer back in 2005</a> found that walking at an average pace for 3 – 5 hours per week had positive effects on survival.<br /><div><br /></div>Pan Pantziarkanoreply@blogger.com0tag:blogger.com,1999:blog-4826023149139426251.post-28687446115932450542015-02-24T20:44:00.000+00:002015-02-24T20:44:25.409+00:00Clarithromycin - a repurposed anticancer drug?An antibiotic may join the ranks of drugs suitable for repurposing as anti-cancer treatments, according to new research from the <a href="http://www.redo-project.org/" target="_blank">Repurposing Drugs in Oncology (ReDO)</a> project published in <a href="http://ecancer.org/journal/journal.php" target="_blank">ecancermedicalscience</a>.<br /><br />Clarithromycin is a very common and effective antibiotic. It is traditionally used for many types of bacterial infections, treatment of Lyme disease and eradication of gastric infection with Helicobacter pylori. It is noted in the World Health Organisation’s list of essential medicines, ensuring it will remain available worldwide at low cost. Dr. Vikas P. Sukhatme of the ReDO project and <a href="http://www.global-cures.org/" target="_blank">GlobalCures</a> says "The multiple mechanisms of action of this drug make it particularly attractive for repurposing."<br /><br />“Clarithromycin is a canonical example of a drug that may have limited antitumor activity on its own, but is extremely valuable against cancer in combination with other drugs,“ says An Van Nuffel, PhD, lead author of the paper and member of the ReDo project and the <a href="http://www.anticancerfund.org/" target="_blank">Anticancer Fund</a>.<br /><br />An international collaboration between anticancer researchers from across the world, the ReDO project is dedicated to promoting the cause of common medicines which may represent an untapped source of novel therapies for cancer.<br /><br />In partnership with ecancer, the ReDO project is publishing a series of papers on drugs with enough evidence to be taken to clinical trials. Future papers will address the potential anti-cancer uses of nitroglycerin, itraconazole and diclofenac.<br /><br />Dr Gauthier Bouche of the ReDO project and the Anticancer Fund describes a serendipitous use of clarithromycin for the treatment of chronic myeloid leukaemia (CML).<br /><br />In 2012, Italian doctors led by Dr Carella prescribed clarithromycin for an infection in a patient with CML. The patient had developed resistance to his treatment, which reversed after treatment with clarithromycin, reinstalled when the drug was discontinued and then reversed again after re-challenge.<br /><br />Low- and middle-income countries (LMIC) may pave the way for drug repurposing. The latest randomised trial done with clarithromycin was done in Egypt, demonstrating that patients with a certain form of lymphoma lived longer when clarithromycin was added to chemotherapy.<br /><br />The faster development of new - but expensive - drugs in High Income Countries may create a role for LMIC to further develop drug repurposing in oncology. Could LMIC with no access to the recent drugs perform trials with clarithromycin?<br /><br />“If clarithromycin were a new drug with the anticancer potential that it has, we would see companies pushing hard for clinical trials and aiming to get to market quickly,” says Pan Pantziarka, PhD, member of the ReDO project and the Anticancer Fund. “Why isn't that happening now in multiple myeloma or resistant leukaemias?”Pan Pantziarkanoreply@blogger.com0tag:blogger.com,1999:blog-4826023149139426251.post-89391859175900593242015-02-19T21:40:00.000+00:002015-02-20T11:01:42.500+00:00Book Review - A Scientist in Wonderland<table border="0" style="width: 100%px;"><tbody><tr><td><b>Keywords:</b> Homeopathy, memoir, medicine<br><b>Title:</b>A Scientist in Wonderland<br><b>Author:</b> Edzard Ernst<br><b>Publisher:</b> Imprint Academic<br><b>ISBN:</b> 978-1845407773 </td> <td></td> <td><div align="center"><img alt="cover" border="1" src="http://images-eu.amazon.com/images/P/1845407776.02.LZZZZZZZ.jpg" height="200" width="150"><br><br><a href="http://www.amazon.com/exec/obidos/ASIN/1845407776/techbookrepor-20"><b>Buy US</b></a><br><a href="http://www.amazon.co.uk/exec/obidos/ASIN/1845407776/454"><b>Buy UK</b></a></div></td></tr></tbody></table>Edzard Ernst initially came to prominence in the UK as Professor of Complementary Medicine, holding the first such chair anywhere in the world. That was in 1993, and Ernst, who already had a pedigree both as a clinician and a researcher, expected that his quest to rigorously apply the scientific method to the various fields of ‘complementary and alternative’ medicine would be welcomed by practitioners and adherents who would want to prove the efficacy of their different ‘modalities’. Now fast forward to 2015 and Ernst is in the public eye once more in the UK with the publication of ‘A Scientist in Wonderland’, his memoir that tells the story not just of his research findings, but also lays bare the meddling of Prince Charles, heir to the British throne and arch-proponent of homeopathy, detoxification theories and a raft of other ‘alternative therapies’.<br><br>The book describes Ernst’s circuitous route to that Professorship – from his unconventional upbringing in post-War Germany, his love of jazz and his hesitant move into medicine. This is an environment in which homeopathy and naturopathy are accepted to a greater extent than in the UK. Indeed his first posting is in Germany’s only homeopathic hospital, where patients seemed to respond well to the endlessly diluted concoctions which are homeopathic medicines. As he points out in graphic detail, there can be not a single molecule of active ingredient left in these medicines, but yet patients recovered. Evidence of effect? Or evidence of the natural evolution of many illnesses and the positive power of the placebo effect? <br><br>In time Ernst moves to more conventional medical institutions. In addition to growing clinical experience he also begins a research career, finding the role of scientist enormously rewarding and intellectually satisfying. His observes, wryly that:<br><br><i>An uncritical scientist is a contradiction in terms: if you meet one, chances are that you have encountered a charlatan. By contrast, a critical clinician is a true rarity, in my experience. If you meet one, chances are that you have found a good and responsible doctor. </i><br><br>There are certainly plenty of patients who will echo that, and indeed it is a complaint that many cancer patients will recognise. Indeed, many of us hope that the Medical Innovation Bill (aka the Saatchi Bill, which Ernst does not support), will encourage more of this critical and scientific thinking in our doctors.<br><br><a href="http://www.anticancer.org.uk/2015/02/book-review-scientist-in-wonderland.html#more">Read more »</a>Pan Pantziarkanoreply@blogger.com0tag:blogger.com,1999:blog-4826023149139426251.post-24295564845898404952015-02-04T10:10:00.001+00:002015-02-04T12:35:34.730+00:00GcMAF Factory RaidedNews from the UK's medical regulator, the MHRA, <a href="https://www.gov.uk/government/news/regulator-warns-against-gcmaf-made-in-unlicensed-facility-in-cambridgeshire" target="_blank">following a raid on the Cambridgeshire lab</a> which was manufacturing GcMAF. This is a blood product that is sold over the internet as a cure for cancer, autism and a host of other conditions. While there is one bona fide early trial on GcMAF on-going in Israel, the product is being sold from a variety of websites as an actual cure. There is no evidence that it is a cure - and the Anticancer Fund of Belgium has been working hard examining the evidence that exists. To date a number of the papers that the people selling GcMAF have been using as 'evidence' have been retracted (withdrawn from the journals in which they were published). There is a good <a href="http://www.anticancerfund.org/news/gcmaf-for-the-treatment-of-breast-cancer-retraction-of-an-article-by-yamamoto-et-al" target="_blank">summary of the evidence at the Anticancer Fund website</a>.<br /><br />In this latest news from the MHRA, concern was raised about the safety of the product:<br /><br /><i>The blood plasma starting material being used to make this drug stated “Not to be administered to humans or used in any drug products”. It was concluded that the production site does not meet Good Manufacturing Practice (GMP) standards and there are concerns over the sterility of the medicine being produced and the equipment being used. There are concerns that the product may be contaminated.</i><br /><br />The conclusion from the MHRA is stark:<br /><br /><i>These products may pose a significant risk to people’s health. Not only were the manufacturing conditions unacceptable but the originating material was not suitable for human use. GcMAF products labelled as ‘First Immune’ are not licensed medicines and have not been tested for quality, safety or effectiveness. People should not start treatment with these specific products. It is important that patients currently taking these products seek their doctor’s advice as soon as possible. People should continue taking prescribed medicines and follow the advice of their doctor.</i><br /><i><br /></i><i><b>Update: The BBC have reported that the government of Guernsey, where many of the companies selling GcMAF are based, has banned the importation of GcMAF.&nbsp;</b></i>Pan Pantziarkanoreply@blogger.com0tag:blogger.com,1999:blog-4826023149139426251.post-13518484343363198392015-02-02T10:56:00.000+00:002015-02-02T10:56:00.450+00:00Open Letter - Medical Innovation BillToday's Daily Telegraph includes an <a href="http://www.telegraph.co.uk/comment/letters/11382880/Letters-NHS-reform-must-be-top-of-each-partys-agenda-ahead-of-the-May-election.html" target="_blank">open letter in support of the Medical Innovation Bill </a>(aka the Saatchi Bill). The letter was conceived and organised independently of the official Saatchi campaign. The letter, which carried 52 signatures, was edited for publication. The full text is reproduced below:<br /><br />------------------------------------------------------------<br /><div align="right" class="MsoNoSpacing" style="text-align: right;"><span style="font-family: Times, Times New Roman, serif; font-size: large;">The Letters Editor<o:p></o:p></span></div><div align="right" class="MsoNoSpacing" style="text-align: right;"><span style="font-family: Times, Times New Roman, serif; font-size: large;">Daily Telegraph<o:p></o:p></span></div><div align="right" class="MsoNoSpacing" style="text-align: right;"><span style="font-family: Times, Times New Roman, serif; font-size: large;">London<o:p></o:p></span></div><div align="right" class="MsoNoSpacing" style="text-align: right;"><span style="font-family: Times, Times New Roman, serif; font-size: large;">29/01/15<o:p></o:p></span></div><div align="right" class="MsoNormal" style="text-align: right;"><br /></div><div class="MsoNormal"><span style="font-family: Times, Times New Roman, serif; font-size: large;">Dear Editor,<o:p></o:p></span></div><div class="MsoNormal"><span style="font-family: Times, Times New Roman, serif; font-size: large;"><br /></span></div><div class="MsoNormal"><span style="font-family: Times, Times New Roman, serif; font-size: large;">We note with considerable interest the successful third reading of the proposed Medical Innovation Bill, aka the Saatchi Bill. While there have been significant advances in cancer treatments in recent decades there remain areas where there has been no meaningful advance. Diseases such as glioblastoma, sarcoma, pancreatic cancer and others have seen no clinically relevant improvements over those same decades. Refractory metastatic solid tumours remain a challenge and a significant cause of morbidity and mortality. Furthermore, for many less common diseases the landscape of clinical trials is barren.<o:p></o:p></span></div><div class="MsoNormal"><span style="font-family: Times, Times New Roman, serif; font-size: large;"><br /></span></div><div class="MsoNormal"><span style="font-family: Times, Times New Roman, serif; font-size: large;">While it is true that clinicians have lee-way to prescribe drugs ‘off-label’, we know from our direct experience with patients that viable clinical options are not being accessed in the vast majority of ‘terminal’ cases. When all standard therapies have failed, and there are no clinical trials available for the patient, the response is almost uniformly to move that patient into palliative care. Too often it appears that clinicians are reluctant to try treatment alternatives – be they metronomic chemotherapies, repurposed non-cancer drugs with evidence of efficacy or compassionate use/medical needs programs. Note that these are all options with often considerable levels of clinical and pre-clinical evidence; this is not junk science or quackery. <o:p></o:p></span></div><div class="MsoNormal"><span style="font-family: Times, Times New Roman, serif; font-size: large;"><br /></span></div><div class="MsoNormal"><span style="font-family: Times, Times New Roman, serif; font-size: large;">We do not dispute that the clinical trial is necessary in order to identify those advances that work and those that do not. However, the evidence base for medicine can come from many different sources. Data collection is a necessary corollary of increased off-label usage and the new registry included in the Bill will record information (including side-effects and outcome data), in every instance of an innovative treatment under the terms of the Bill. This ground-breaking registry will enable us to mine and analyse real world data so that we are not dealing with a set of anecdotes, but validated and clinically useful information and so providing greater patient protection than exists at present. Physicians treating patients with no other options would be empowered to evaluate off-label interventions with the highest evidence of efficacy. <o:p></o:p></span></div><div class="MsoNormal"><span style="font-family: Times, Times New Roman, serif; font-size: large;"><br /></span></div><div class="MsoNormal"><span style="font-family: Times, Times New Roman, serif; font-size: large;">The reluctance of physicians to explore alternative options may not be solely due to a fear of litigation, as Lord Saatchi contends. There are other social, cultural and institutional barriers at work – individual and institutional comfort zones – which often preclude off-label prescribing. However, if the passing of the Bill affects a change in thinking such that there is a greater willingness to explore potentially helpful treatments, then it will have provided benefit to patients. Passing the Bill sends a positive message that encourages responsible use of off-label options. Not passing the Bill sends a strong negative signal that off-label usage is neither encouraged nor supported.<o:p></o:p></span></div><div class="MsoNormal"><span style="font-family: Times, Times New Roman, serif; font-size: large;"><br /></span></div><div class="MsoNormal"><span style="font-family: Times, Times New Roman, serif; font-size: large;">Ultimately the question that must be addressed is: what can we responsibly offer to those patients for whom there are no suitable clinical trials? <o:p></o:p></span></div><div class="MsoNormal"><span style="font-family: Times, Times New Roman, serif; font-size: large;"><br /></span></div><div class="MsoNormal"><span style="font-family: Times, Times New Roman, serif; font-size: large;">Yours Sincerely,<o:p></o:p></span></div><div class="MsoNormal"></div><ul><li><span style="font-family: Times, 'Times New Roman', serif;"><span style="font-size: large;">Pan Pantziarka PhD, The George Pantziarka TP53 Trust, London (UK) &amp; Anticancer Fund, Brussels (Belgium)</span></span></li><li><span style="font-family: Times, 'Times New Roman', serif;"><span style="font-size: large;">Dominic Hill - www.survivingterminalcancer.com Film maker &amp; patient advocate (UK)</span></span></li><li><span style="font-family: Times, 'Times New Roman', serif;"><span style="font-size: large;">Professor Marc-Eric Halatsch, Oncological Neurosurgeon and Professor of Neurosurgery, University of Ulm (Germany)</span></span></li><li><span style="font-family: Times, 'Times New Roman', serif;"><span style="font-size: large;">Lydie Meheus PhD, Managing Director, Anticancer Fund, Brussels (Belgium)</span></span></li><li><span style="font-family: Times, 'Times New Roman', serif;"><span style="font-size: large;">Dr. Gauthier Bouche, Medical Director, Anticancer Fund, Brussels (Belgium)</span></span></li><li><span style="font-family: Times, 'Times New Roman', serif;"><span style="font-size: large;">Richard Gerber, PhD, long-term glioblastoma survivor and patient advocate (Italy)</span></span></li><li><span style="font-family: Times, 'Times New Roman', serif;"><span style="font-size: large;">Professor Angus Dalgleish, St George's Hospital, University of London (UK)</span></span></li><li><span style="font-family: Times, 'Times New Roman', serif;"><span style="font-size: large;">Professor Ahmed Ashour Ahmed, Professor of Gynaecological Oncology, University of Oxford, Consultant Gynaecological Oncology Surgeon (UK)</span></span></li><li><span style="font-family: Times, 'Times New Roman', serif;"><span style="font-size: large;">James Hargrave, Empower Access to Medicine (UK)</span></span></li><li><span style="font-family: Times, 'Times New Roman', serif;"><span style="font-size: large;">Dr John Symons, Director, Cancer of Unknown Primary Foundation (UK)</span></span></li><li><span style="font-family: Times, 'Times New Roman', serif;"><span style="font-size: large;">Flóra Raffai, Findacure (UK)</span></span></li><li><span style="font-family: Times, 'Times New Roman', serif;"><span style="font-size: large;">Professor Stephen Kennedy, Professor of Reproductive Medicine, University of Oxford (UK)</span></span></li><li><span style="font-family: Times, 'Times New Roman', serif;"><span style="font-size: large;">Dr Ian N Hampson, Reader in Viral Oncology, University of Manchester (UK)</span></span></li><li><span style="font-family: Times, 'Times New Roman', serif;"><span style="font-size: large;">Professor Andy Hall, Associate Dean of Translational Research, Newcastle University (UK)</span></span></li><li><span style="font-family: Times, 'Times New Roman', serif;"><span style="font-size: large;">Professor Emeritus Ben A. Williams, Psychology, long-term glioblastoma survivor, patient advocate, Moore’s Cancer Center, University of California, San Diego (USA)</span></span></li><li><span style="font-family: Times, 'Times New Roman', serif;"><span style="font-size: large;">Dr Al Musella, President, Musella Foundation, founder The Grey Ribbon crusade: umbrella organisation for over 100 brain cancer charities (USA)</span></span></li><li><span style="font-family: Times, 'Times New Roman', serif;"><span style="font-size: large;">Professor John Boockvar, Director, Brain Tumor Center Lenox Hill Hospital NYC, Professor of Neurosurgery (USA)</span></span></li><li><span style="font-family: Times, 'Times New Roman', serif;"><span style="font-size: large;">Professor Emil J Freireich, Ruth Harriet Ainsworth Chair, Developmental Therapeutics, The University of Texas MD Anderson Cancer Center, Houston, Texas (USA)</span></span></li><li><span style="font-family: Times, 'Times New Roman', serif;"><span style="font-size: large;">Brett Shockley - patient advocate (USA)</span></span></li><li><span style="font-family: Times, 'Times New Roman', serif;"><span style="font-size: large;">Professor David Walker, Professor Pediatric Oncology, University of Nottingham (UK)</span></span></li><li><span style="font-family: Times, 'Times New Roman', serif;"><span style="font-size: large;">Laura Mancini, PhD, Clinical Scientist, National Hospital for Neurology and Neurosurgery, UCLH NHS Foundation Trust, London (UK)</span></span></li><li><span style="font-family: Times, 'Times New Roman', serif;"><span style="font-size: large;">John Morrissey, Adviser to the Childrens Cancer Research Fund (USA)</span></span></li><li><span style="font-family: Times, 'Times New Roman', serif;"><span style="font-size: large;">Stephen Western, patient advocate, Astrocytomaoptions.com (Canada)</span></span></li><li><span style="font-family: Times, 'Times New Roman', serif;"><span style="font-size: large;">Richard E. Kast, MD, IIAIGC Study Center (USA)</span></span></li><li><span style="font-family: Times, 'Times New Roman', serif;"><span style="font-size: large;">Charlie Chan DPhil FRCS, Consultant Breast Surgeon (UK)</span></span></li><li><span style="font-family: Times, 'Times New Roman', serif;"><span style="font-size: large;">Professor Chas Bountra, Professor of Translational Medicine, University of Oxford (UK)</span></span></li><li><span style="font-family: Times, 'Times New Roman', serif;"><span style="font-size: large;">Dr Henrietta Morton-King, North Cumbria University Hospitals Trust (UK)</span></span></li><li><span style="font-family: Times, 'Times New Roman', serif;"><span style="font-size: large;">Dr Andrew Brunskill, Clinical Assistant Professor of Epidemiology and Health Services, University of Washington Seattle (USA)</span></span></li><li><span style="font-family: Times, 'Times New Roman', serif;"><span style="font-size: large;">Vincent Galbiati, President &amp; CEO of Tomorrow’s Cures Today, Washington DC (USA)</span></span></li><li><span style="font-family: Times, 'Times New Roman', serif;"><span style="font-size: large;">Neil Hutchison, Founder - Magic Water Pediatric Cancer Foundation - San Diego (USA)</span></span></li><li><span style="font-family: Times, 'Times New Roman', serif;"><span style="font-size: large;">Fiona Court, Consultant Oncoplastic Breast Surgeon, Cheltenham (UK)</span></span></li><li><span style="font-family: Times, 'Times New Roman', serif;"><span style="font-size: large;">Professor Alastair Buchan, Head of the Medical Science Division and the Dean of the Medical School at the University of Oxford (UK)</span></span></li><li><span style="font-family: Times, 'Times New Roman', serif;"><span style="font-size: large;">Dr. Georgios Evangelopoulos, patient advocate, lawyer &amp; political scientist (Greece)</span></span></li><li><span style="font-family: Times, 'Times New Roman', serif;"><span style="font-size: large;">Professor John Yarnold, Professor of Clinical Oncology at The Royal Marsden and Institute of Cancer Research (UK)</span></span></li><li><span style="font-family: Times, 'Times New Roman', serif;"><span style="font-size: large;">Professor Jerome H Pereira, Consultant General &amp; Oncoplastic Breast Surgeon, Norwich Medical School University of East Anglia (UK)</span></span></li><li><span style="font-family: Times, 'Times New Roman', serif;"><span style="font-size: large;">Dr Lynne Hampson, Non Clinical Lecturer in Oncology, Institute of Cancer Sciences, Manchester (UK)</span></span></li><li><span style="font-family: Times, 'Times New Roman', serif;"><span style="font-size: large;">Professor Robert Kirby, MD, FRCS, Consultant Surgeon and UHNM Hospital Dean (UK)</span></span></li><li><span style="font-family: Times, 'Times New Roman', serif;"><span style="font-size: large;">Professor Gareth Evans, Professor of Medical Genetics and Cancer Epidemiology, University of Manchester (UK)</span></span></li><li><span style="font-family: Times, 'Times New Roman', serif;"><span style="font-size: large;">Dr Rupert McShane, Coordinating Editor Cochrane Dementia and Cognitive Improvement Group, Oxford University (UK)</span></span></li><li><span style="font-family: Times, 'Times New Roman', serif;"><span style="font-size: large;">Michael Shackcloth, Consultant Thoracic Surgeon, Liverpool Heart and Chest Hospital (UK)</span></span></li><li><span style="font-family: Times, 'Times New Roman', serif;"><span style="font-size: large;">Professor Vikas P. Sukhatme, Professor of Medicine, Harvard Medical School, Co-founder Global Cures (USA)</span></span></li><li><span style="font-family: Times, 'Times New Roman', serif;"><span style="font-size: large;">Vidula Sukhatme, Co-founder Global Cures (USA)</span></span></li><li><span style="font-family: Times, 'Times New Roman', serif;"><span style="font-size: large;">Sarah Lindsell – CEO, The Brain Tumour Charity (UK)</span></span></li><li><span style="font-family: Times, 'Times New Roman', serif;"><span style="font-size: large;">Neil Dickson - Chairman, The Brain Tumour Charity (UK)</span></span></li><li><span style="font-family: Times, 'Times New Roman', serif;"><span style="font-size: large;">Alex Smith (Founder, Harrison’s Fund) (UK)</span></span></li><li><span style="font-family: Times, 'Times New Roman', serif;"><span style="font-size: large;">Giles Cunnick, Consultant General &amp; Breast Surgeon, Bucks Healthcare NHS Trust, (UK)</span></span></li><li><span style="font-family: Times, 'Times New Roman', serif;"><span style="font-size: large;">Dr Piers Mahon, Biotech Consultant, (UK)</span></span></li><li><span style="font-family: Times, 'Times New Roman', serif;"><span style="font-size: large;">Paul Fitzpatrick, Chairman, Duchenne Now, (UK)</span></span></li><li><span style="font-family: Times, 'Times New Roman', serif;"><span style="font-size: large;">Dr David Faurrugia, Consultant Oncologist, Cheltenham General Hospital (UK)</span></span></li><li><span style="font-family: Times, 'Times New Roman', serif;"><span style="font-size: large;">Dr Chris Govender, Medical Officer in Addictions, (UK)</span></span></li><li><span style="font-family: Times, 'Times New Roman', serif;"><span style="font-size: large;">Sue Farrington Smith, Chief Executive, Brain Tumour Research, (UK)</span></span></li><li><span style="font-family: Times, 'Times New Roman', serif;"><span style="font-size: large;">Professor Steven Gill, Professor in Neurosurgery, University of Bristol (UK)</span></span></li></ul><br /> <br /><div class="MsoNormal"><o:p></o:p></div>Pan Pantziarkanoreply@blogger.com0tag:blogger.com,1999:blog-4826023149139426251.post-38078415773124562432015-01-21T08:18:00.001+00:002015-01-21T08:20:34.201+00:00Live Blood Analysis - A Scam<a href="http://www.anticancer.org.uk/2014/05/the-case-of-dr-henry-mannings.html">Dr Henry Mannings</a>, who went through hell with the General Medical Council last year after facing groundless accusations from a vindictive consultant oncologist who objected to what the Star Throwers charity was telling his patients, recently sent me a price list from a well-known private clinic that specialises in treating cancer patients. What was shocking to us was not just the prices charged but that this clinic offered patients a service called &#39;live blood analysis&#39;. Like Dr Mannings I am astounded that any reputable doctor would be offering this to patients, but it is offered and it&#39;s not cheap. So, for those who might be interested, just what is &#39;live blood analysis&#39; (LBA) and is there any evidence that it is useful?<br><br>LBA, (which is sometimes called Hemaview, live cell analysis or nutritional blood analysis) is a procedure that involves taking a sample of blood, putting it on a slide and taking a look at it using a microscope. From this it is claimed that a skilled LBA practitioner can detect cancer, immune disorders, yeast and bacterial infections and a spread of other conditions. Patients will be told that the cells are not moving about in the correct way, or that they look abnormal or are showing signs of fermentation or infection and so on. Patients will be told that conventional blood tests cannot capture many of these issues because they do not look at live cells in motion. A lot of scientific sounding terminology will be used along the way, and of course the microscope is a scientific instrument so all of this must be based on fact, right? Wrong.<br><br>There is no scientific evidence for LBA. It is junk science - something dressed up to look like science but not based on any evidence or credible scientific theory.<br><br><a href="http://www.anticancer.org.uk/2015/01/live-blood-analysis-scam.html#more">Read more »</a>Pan Pantziarkanoreply@blogger.com0tag:blogger.com,1999:blog-4826023149139426251.post-14857975073592308442015-01-13T21:16:00.002+00:002015-01-13T21:16:50.356+00:00Book Review - 'Being Mortal' by Atul Gawande<table border="0" style="width: 100%px;"><tbody><tr> <td><b>Keywords:</b> Cancer, aging, medicine<br /><b>Title:</b>Being Mortal: Illness, Medicine and What Matters in the End<br /><b>Author:</b> Atul Gawande<br /><b>Publisher:</b> Profile Books<br /><b>ISBN:</b> 978-1846685811 </td> <td></td> <td><div align="center"><img alt="cover" border="1" src="http://images-eu.amazon.com/images/P/1846685818.02.LZZZZZZZ.jpg" height="200" width="150" /><br /><br /><a href="http://www.amazon.com/exec/obidos/ASIN/1472910516/techbookrepor-20"><b>Buy US</b></a><br /><a href="http://www.amazon.co.uk/exec/obidos/ASIN/1472910516/454"><b>Buy UK</b></a></div></td></tr></tbody></table><br />In 'Being Mortal' Atul Gawande asks a series of difficult, important but uncomfortable questions about the nature of medicine and mortality. These are tricky waters to navigate, but essential all the same as it gets to the heart of what it is we want medicine to do for us. But navigate them we must, both because we have an aging population that often faces impossible choices regarding social care and also in the context of increasing cancer incidence (one of the consequences of that aging).<br /><br />The author, a practicing doctor, uses the experiences of family, friends and patients alike to illustrate the choices that face us both in aging and in cancer care. He skilfully weaves in these experiences and in doing so puts complex problems into real situations so that he explore the options available, the things we want and cannot have and also, just importantly, draws out the underlying questions. He explores the history and evolution of patient care, how changes in the pattern of work and family life have impacted our expectations of old age. The contrasts between what we want in terms of autonomy and quality of life on the one hand, and what our medical and social care systems provides on the other are brought sharply into life. For those of us who have had to navigate these problems for elderly relatives it is familiar territory outlined with a thought-provoking honesty.<br /><br />In terms of cancer the problems are starker still. When treatments fail what do we want to do? We are up against the limits of what medicine can deliver. Up against what our medical systems can cope with. The dilemma here is to risk cripplingly expensive new treatments, often with horrendous side effects or to opt instead for palliative or hospice care. These are hard choices to make, assuming we are given the choices in the first place. Sometimes there are less toxic options to try, but many doctors seem to prefer to go for the toxic chemotherapy route rather than step back and look at what the patient wants.<br /><br />If there’s a theme that jumps out from this book it is that we need to be moving to a different model of the patient-doctor relationship. Dr Gawande describes this admirably. There is the doctor as expert doling out wisdom from on high. There is the doctor as information source giving facts and figures impartially to patients ill-equipped to come to a decision. And then there is the hardest option of all, which is the doctor as partner to the patient. A doctor who engages with the patient to discover what it is that is most important to them and then to help the patient make the choices that deliver the best compromises that are possible. Unfortunately many doctors are simply not trained or don’t have the tools to take this role, which is hard on the patients but hard too for the doctors.<br /><br />While this is a challenging book at times, it is never sentimental or emotive, it’s humane and concerned. Medical systems the world over are in flux, struggling to cope with the increases in demand that our successes in medicine have delivered. In many ways we should not lose sight of how much progress we have made. But neither should we be happy with the status quo that leaves so many patients poorly served. Something has to give. And perhaps part of what has to give is that old-fashioned view of the doctor as expert, with the patient as passive receiver of care with no say in their own treatment.<br /><br />Pan Pantziarkanoreply@blogger.com0tag:blogger.com,1999:blog-4826023149139426251.post-2651064208952452812014-12-22T21:32:00.000+00:002014-12-22T21:32:57.931+00:00When less is more<div class="MsoNormal">The conventional approach to chemotherapy treatment for cancer is to give the patient a cocktail of different chemo drugs at the maximum tolerated dose (MTD). The idea of MTD treatment is to hit the cancer with the most toxic treatment the patient can stand in the hope that it causes the maximum damage to the disease. Normally a treatment consists of a number of cycles of chemo using a mix of drugs, with the idea that each drug will attack the tumour in a different way – reducing the chance of the tumour surviving the onslaught. And it’s an onslaught for the person receiving the treatment too – most chemotherapy drugs are toxic to a wide range of cells, not just cancer cells. Hence the hair loss, the nausea, the immune suppression, fatigue and the rest of the side effects that makes chemo so hard.<o:p></o:p></div><div class="MsoNormal"><br></div><div class="MsoNormal">Of necessity a person needs recovery time after each cycle of chemotherapy. Blood counts need to recover, sickness needs to pass, people need to regain some strength. Unfortunately that’s recovery time that tumours can also use to recover. The highest rates of tumour kill tend to be at the least cycles, the later cycles tend to be less effective, particularly if resistance starts to kick in.<o:p></o:p></div><div class="MsoNormal"><br></div><div class="MsoNormal">However, this isn&#39;t the only way of delivering treatment. An alternative approach to chemotherapy has been developing for some time. Low dose metronomic chemotherapy involves many of the same drugs as MTD chemo, but delivered at low doses, often in tablet form, but with no treatment breaks. The continuous dosing is possible because at these low doses the drugs work in very different ways to when they are delivered at MTD levels. The side effects are minimal as the drugs are no longer acting as potent toxins to massively kill cells. <o:p></o:p></div><div class="MsoNormal"><br></div><a href="http://www.anticancer.org.uk/2014/12/when-less-is-more.html#more">Read more »</a>Pan Pantziarkanoreply@blogger.com0tag:blogger.com,1999:blog-4826023149139426251.post-1519738894943528512014-12-15T20:49:00.004+00:002014-12-15T20:49:47.075+00:00Saatchi Bill and Medical Anecdotes<div class="MsoNormal">Opponents of the Medical Innovation Bill (aka as the Saatchi Bill), such as Sarah Wollaston MP, have been very vocal in attacking the Bill by making a number of false claims about what the Bill will do. One such argument is that the Bill will undermine medical progress by doing away with clinical trials, and that instead we will just have to rely on individual anecdotes that arise from doctors using innovative off-label treatments on patients. In fact Sarah Wollaston even referred to the Bill as the ‘Medical Anecdotes Bill’ in her recent speech in the House of Commons.<o:p></o:p></div><div class="MsoNormal"><br></div><div class="MsoNormal">There are a number of points that to raise in response to this false assertion.<o:p></o:p></div><div class="MsoNormal"><br></div><div class="MsoNormal">First, there is no intention to replace clinical trials. The Bill is about treating patients with no place left to turn – these are people who have exhausted standard therapies and for whom there are few options left to explore. If a clinical trial is open and the patient is eligible then that is the place to go if it is in the patient’s best interest. There may be cases where it is the right thing to do, just as there are cases when it will not benefit the patient who is offered the additional choice of an non-standard treatment (for example an off-label drug with evidence of clinical activity in the patient’s illness). This will be decided on a case by case basis, what it will not do is force doctors to ignore clinical trials or undermine the trials process.<o:p></o:p></div><div class="MsoNormal"></div><a href="http://www.anticancer.org.uk/2014/12/saatchi-bill-and-medical-anecdotes.html#more">Read more »</a>Pan Pantziarkanoreply@blogger.com36tag:blogger.com,1999:blog-4826023149139426251.post-70719152372978840942014-12-12T07:44:00.001+00:002014-12-12T07:44:24.561+00:00Not All Journals Are Created EqualAn increasing hazard in science publishing is the increasing number of &#39;predatory journals&#39;. The term refers to low-quality scientific journals which exist solely to make easy money under the &#39;author pays&#39; model of publishing. These journals pretend to do peer review and they look and feel like proper academic journals, but in reality they will publish anything to harvest those publication fees. It&#39;s a scam, and a successful one given the growth of the number of these journals. The way the scam works is for these journals to solicit papers, to claim they do peer review, then to accept the papers. The authors are billed the article processing and publication fees, and then the paper is published online.<br><br>There are multiple dangers in this process. The first and most obvious is that the authors are ripped off - they have effectively just paid for someone to turn there text into a web page. There has been no peer review, no proper scrutiny of the content and the chances are that the paper will be ignored by other academics. If you have a limited budget for publication fees you&#39;ve just wasted it. If you are starting out in your research career publishing in these journals may seem an easy route to getting some papers to your name, but more knowledgeable colleagues will know what you&#39;ve done and so the risk is that you damage your career, not enhance it. It is also possible that unscrupulous academics will deliberately use predatory journals to beef up a CV to impress people who don&#39;t know about predatory journals - all of which sound eminently respectable to the unsuspecting.<br><br>However, the biggest danger is not with academics, but with the general public. Most people are impressed by a paper that is published in a scientific journal. Scammers and snake-oil salesmen can use this to peddle fake medical treatments to desperate patients. Shoddy papers that sound scientifically plausible can be published in predatory journals and then used to convince people that there&#39;s some real science behind the scam. If you&#39;re not a scientist or someone versed in the medical literature a paper that claims to treat late stage cancer patients and to have miraculous results can be very convincing. The best examples of this are the scammers selling GcMAF as a miracle cure for cancer, autism, AIDS and just about everything else.<br><br>How can you, as a reader, verify that the journal paper you are reading is not a piece of junk published in exchange for a few hundred dollars?<br><br><a href="http://www.anticancer.org.uk/2014/12/not-all-journals-are-created-equal.html#more">Read more »</a>Pan Pantziarkanoreply@blogger.com0tag:blogger.com,1999:blog-4826023149139426251.post-59832941059982550652014-11-27T20:36:00.000+00:002014-11-27T20:36:09.507+00:00Alveolar Soft Part Sarcoma - The Reverse Warburg Effect In Action?Alveolar soft part sarcoma (ASPS) is a rare cancer - rare even among soft tissue sarcomas - that is slow growing but hard to treat. When the disease metastasises the prognosis is generally grim and there are few options for treatment if surgical resection is not possible. A new paper, published in the journal Cancer Cell, describes work in a mouse model of the disease which may ultimately have important therapeutic consequences.<br /><br />A team at the University of Utah have created a mouse model of ASPS, by fusing two strands of DNA to create a fusion gene which forms tumours in the mice in which it is implanted. What's more the resulting disease behaves very much like ASPS in humans, including producing very similar genetic profiles. Intriguingly the mouse tumours formed preferentially in areas of the body which had high concentrations of lactate. In humans this tends to be in the skeletal muscles as lactate is a by-product when our muscles are straining for energy in low oxygen conditions. In the mice the areas with the highest lactate concentrations were in the skull.<br /><br />Generally tumours are believed to generate excess lactate as a by-product of their metabolism - this is known as the Warburg effect. And yet here the tumours seem to be feeding off the lactate produced by non-cancer cells. As one of the researchers, Kevin Jones explains: "It's unusual to find a cancer using lactate this way. The ASPS cells grow preferentially where they are bathed in high concentrations of lactate."<br /><br />The most likely explanation is that this is yet another example of the <a href="http://www.anticancer.org.uk/2012/03/reverse-warburg-effect-and-breast.html" target="_blank">reverse Warburg effect</a>, first described by Michael Lisanti and his team. This is a topic of huge importance as it revises what has been seen as a core component of our understanding of cancer. In this model of cancer, the tumour cells act on non-cancer cells to change their metabolism so that they emit lactate and glutamine, which the tumour cells use as a more powerful fuel source.<br /><br />This does open up opportunities for intervention, however. If we can interrupt that 'metabolic shuttle' between lactate consuming tumour cells and stromal cells they are 'farming' then we can starve the cancer cells and so slow - or possibly even halt - tumour growth.<br /><div><br /></div>Pan Pantziarkanoreply@blogger.com1tag:blogger.com,1999:blog-4826023149139426251.post-80613375531184284842014-11-27T10:42:00.002+00:002014-11-27T11:04:02.138+00:00Cimetidine as an anticancer drug - New ReDO paper<span style="font-family: Helvetica Neue, Arial, Helvetica, sans-serif;">The latest paper from the <a href="http://www.anticancer.org.uk/2014/07/redo-repurposing-drugs-in-oncology.html" target="_blank">ReDO project</a> has just been published. Our focus for this paper is the well-known antacid cimetidine (trade name Tagamet, but now available as a generic). The paper summarises the extensive pre-clinical and clinical evidence that shows cimetidine has huge potential in cancer treatment. It has multiple mechanisms of action and there is clinical trial evidence that it is associated with a survival in colorectal cancers.</span><br><span style="font-family: Helvetica Neue, Arial, Helvetica, sans-serif;"><br></span><span style="font-family: Helvetica Neue, Arial, Helvetica, sans-serif;">The paper is published as open access at the journal <a href="http://ecancer.org/journal/8/full/485-repurposing-drugs-in-oncology-redo-cimetidine-as-an-anti-cancer-agent.php" target="_blank">ecancer</a>.</span><br><span style="font-family: Helvetica Neue, Arial, Helvetica, sans-serif;"><br></span><span style="font-family: Helvetica Neue, Arial, Helvetica, sans-serif;">The press release provides a few more details:</span><br><br><div align="center" class="MsoNormal" style="background-color: white; color: #222222; font-family: &#39;Times New Roman&#39;, serif; font-size: 12pt; margin: 0cm 0cm 0.0001pt; text-align: center;"><span style="color: black; font-family: Arial, sans-serif; font-size: 16pt;">How a common antacid could lead to cheaper anti-cancer drugs<u></u><u></u></span></div><div align="center" style="background-color: white; color: #222222; font-family: &#39;Times New Roman&#39;, serif; font-size: 12pt; margin: 0cm 0cm 0.0001pt; text-align: center;"><br></div><div style="background-color: white; color: #222222; font-family: arial, sans-serif; font-size: 13px;"><div style="font-family: &#39;Times New Roman&#39;, serif; font-size: 12pt; margin: 0cm 0cm 0.0001pt; text-align: justify;"><strong><span style="color: black; font-family: Calibri, sans-serif; font-size: 14pt;">The cancer solution in your medicine cabinet</span></strong><span style="color: black; font-family: Calibri, sans-serif; font-size: 14pt;"><u></u><u></u></span></div><div style="font-family: &#39;Times New Roman&#39;, serif; font-size: 12pt; margin: 0cm 0cm 0.0001pt; text-align: justify;"><br></div><div style="font-family: &#39;Times New Roman&#39;, serif; font-size: 12pt; margin: 0cm 0cm 0.0001pt; text-align: justify;"><span style="color: black; font-family: Calibri, sans-serif; font-size: 14pt;">A popular indigestion medication can increase survival in colorectal cancer, according to research published in <em>e</em>cancermedicalscience. But in fact, scientists have studied this for years - and a group of cancer advocates want to know why this research isn&#39;t more widely used.<u></u><u></u></span></div><div style="font-family: &#39;Times New Roman&#39;, serif; font-size: 12pt; margin: 0cm 0cm 0.0001pt; text-align: justify;"><br></div><div style="font-family: &#39;Times New Roman&#39;, serif; font-size: 12pt; margin: 0cm 0cm 0.0001pt; text-align: justify;"><span style="color: black; font-family: Calibri, sans-serif; font-size: 14pt;">&quot;Cimetidine is an interesting drug as it&#39;s very safe, very well-known, and has clinical results in cancer that have been confirmed in a number of trials,&quot; says Pan Pantziarka, lead author of the paper and member of the Repurposing Drugs in Oncology (ReDO) project.<u></u><u></u></span></div><div style="font-family: &#39;Times New Roman&#39;, serif; font-size: 12pt; margin: 0cm 0cm 0.0001pt; text-align: justify;"></div></div><a href="http://www.anticancer.org.uk/2014/11/cimetidine-as-anticancer-drug-new-redo.html#more">Read more »</a>Pan Pantziarkanoreply@blogger.com0